TREM-1 factor:
Triggering receptors expressed on myeloid cells-1 is a key inflammatory
amplifier that interacts with a number of TLR pathways depending on the
severity of the inflammatory condition (He, Yang, Wang, Jia, Xie &
Zhou, 2019; Youssef et al., 2009). According to Sun et al’s research,
TREM-1 was first revealed to be produced in the context of SAH and has
been linked to the pathogenesis of BBB disruption. This is one of EBI’s
most serious pathological symptoms (Sun, Duan, Jing, Wang, Hou & Zhang,
2019; Sun, Ma, Jing, Wang, Hao & Wang, 2017a; Sun, Ma, Jing, Wang, Hao
& Wang, 2017b). According to a new research, TREM-1 is necessary for
SYK mobilization and downstream activation of CARD9/NF-κB and
NLRP3/caspase-1 in microglia following stroke (Xu et al., 2019a) .
TREM-1 inhibition by LP17 significantly reduced the severity of EBI, and
the protective effects were attributed to reduction of downstream
p38MAPK/MMP-9 activation and hence ZO-1 preservation (Sun, Duan, Jing,
Wang, Hou & Zhang, 2019). TREM-1 activation can be inhibited by fusion
proteins or synthetic inhibitory peptides, which can reduce the
production of pro-inflammatory mediators and leukocyte recruitment
(Boufenzer et al., 2015; Schenk, Bouchon, Seibold & Mueller, 2007).
Neuroinflammation has been linked to post-stroke impairment in the past
(Yirmiya & Goshen, 2011). According to the findings of (Xu et al.,
2019a) , inhibiting TREM-1 improves long-term neurobehavioral deficits
in the hippocampus following ischemic stroke by boosting cell
proliferation and synaptic plasticity. According to the evidence
described above, TREM-1 may have a role in the inflammatory pathways
that contribute to EBI after SAH.